Approximately 5-7 million Americans are afflicted with chronic skin wounds that account for billions of dollars in medical expenses each year.1,2 The incidence of chronic wounds is expected to increase dramatically3 due to an increased elderly population and incidence of diabetes, a disease that is accompanied by wound-healing deficiencies.4 In the United States, at least 82,000 lower-limb amputations are performed annually due to diabetic ulcers.5 
Cell migration is an essential event in wound repair throughout the body. In tissues ranging from skin to blood vessels to bone, the migration of cells is critical for healing and regeneration.6-8. In dermal tissue repair, the migration of keratinocytes from the wound edges helps to close the wound, with re-epithelialization viewed as a hallmark of successful wound care. Early re-epithelialization initiates wound remodeling within the underlying granulation tissue, and early wound closure reduces the chance of developing hypertrophic scarring or other related problems.9 Growth factors and other mitogens often provide the molecular cues that induce cell migration.10 Growth factor deficiencies lead to impaired wound healing, as reduced levels of numerous growth factors have been observed in chronic wounds when compared with normal acute wounds.11-13 
One of the most important factors in epidermal cell growth and migration is epidermal growth factor (EGF).6,14 EGF is released in abundance by platelets at the wound site and is one of several growth factors that are deficient in chronic wounds. This growth factor has been credited with playing a prominent role in wound closure through stimulation of epithelial cell migration and proliferation; EGF also reduces scarring by preventing excessive wound contraction.15 Accordingly, cell migration directed by one or more growth factors is a critical element in wound healing, and it is believed that the ability to control the migration direction of cells will lead to accelerated closure of wounds.
Commonly used approaches to treat chronic or acute wounds are typically based on simple wound care regimens involving debridement, cleaning, and application of moist dressings.16 More advanced dressings such as growth factor-containing topical gels17,18 have met with only limited clinical success, largely due to the inadequate delivery and persistence of the growth factor at the wound site.19 Many growth factors, including EGF, require prolonged exposure to cells in order to elicit a response,20 explaining why a single topical growth factor application often fails. Topically applied agents, such as growth factors, are rapidly washed off the wound by exudation or absorbed into the wound dressing. In fact, the available amount of topically applied basic fibroblast growth factor in solution decreases by 50% within 4 hours of contact with sterile gauze,21 and reapplication of growth factors is often cost prohibitive. Furthermore, growth factors in the physiological environment can be rapidly degraded or otherwise rendered inactive before reaching their target.
Covalent tethering of growth factors to biomaterials has the potential to ameliorate many of these problems, and possibly result in increased availability of active growth migration signals, coupled with precise control over cell migration direction. Patterning polymeric surfaces with bioactive molecules is becoming an attractive method for gaining specific control over cell adhesion and exploring cell function.22-26 While the majority of patterning research has involved the creation of cell adhesion templates via patterning of peptide sequences or matrix proteins,22-24 it is also possible to pattern-immobilize growth factors in the same manner.25,27 Previous studies have shown that EGF retains its biological activity following chemical modification with photoactive molecules and surface immobilization via exposure to long-wavelength ultraviolet (UV) light.28 In fact, immobilized EGF has proven to be more mitogenic for Chinese hamster ovary cells than free EGF.28 This result is hypothesized to be due to the inability of cells to internalize immobilized EGF, a process that would normally lead to consumption of the growth factor and down-regulation of its receptors.
Acceleration of wound closure not only results in decreased patient suffering and cost of wound treatment but may also minimize scarring and lead to formation of a more stable closed wound.9,34 A recent review of the use of growth factors in wound dressings concluded that the clinical outcomes of these materials have been “generally disappointing.”17 It is widely accepted that these lackluster results have been directly attributable to the manner in which growth factors were incorporated into the dressings, namely that the delivery methods did not allow for sustained growth factor availability or bioactivity. Thus, materials that deliver bioactive molecules in a manner that prolongs their availability and bioactivity would possess a significant advantage over existing dressings.
Moreover, providing a means to actively guide the direction or speed of cell migration would also have significant consequences for improvement of wound-healing therapies. Another major obstacle in implementing growth factor-based therapies has been the expense of the biomolecules, meaning that a system that improves healing responses using a reduced amount of growth factor could make growth factor based wound healing therapies more widely available. Therefore, there is a long felt need in the medical community for improved materials and methods that overcome one or more of the above-described obstacles in treating chronic wounds.